Evidence map›Paper›PMID 32913506›Full record

ArticleAmerican journal of translational research2020

Long non-coding RNA LINC01116 is overexpressed in lung adenocarcinoma and promotes tumor proliferation and metastasis.

Lizhong Zeng, Xin Lyu, Jingyan Yuan, Wei Wang, Nannan Zhao, Boxuan Liu, Ruiying Sun, Xia Meng, Shuanying Yang

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Computational Resources for Studying miRNA-lncRNA Interactions.Methods in molecular biology (Clifton, N.J.) · 2026
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  20. Promising Advances in LINC01116 Related to Cancer.Frontiers in cell and developmental biology · 2021
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Lizhong ZengDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Xin LyuDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Jingyan YuanDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Wei WangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Nannan ZhaoDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Boxuan LiuDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Ruiying SunDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Xia MengDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Shuanying YangDepartment of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University Xi'an, Shaanxi, China.
Second Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long non-coding RNA LINC01116 is involved in the occurrence and progression of a variety of cancers. However, the specific role of LINC01116 in lung adenocarcinoma (LUAD) remains unclear. In this work, we found that LINC01116 was overexpressed in LUAD tissues and cell lines and that increased expression was significantly associated with worse prognoses in patients with LUAD. Univariate and multivariate Cox regression analyses indicated that LINC01116 was an independent risk factor for the prognosis of patients with LUAD. Downregulation of LINC01116 significantly inhibited cell proliferation and migration, promoted cell apoptosis, and prevented cell progression from G1 to S phase. In addition, downregulation of LINC01116 significantly inhibited the epithelial-mesenchymal transition, leading to an increased expression of the epithelial marker E-cadherin and decreased expression of the mesenchymal markers N-cadherin and vimentin. In summary, our results suggest that LINC01116 may act as an oncogene in LUAD and may be a valuable prognostic biomarker for patients with LUAD.

Indexed as

EMTLINC01116lung adenocarcinomaprognosisproliferation

Identifiers

PMID32913506
PMCPMC7476163
OpenAlexW3086673373

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.